We propose that the interaction between Rictor and p53 is critical in hepatocarcinogenesis and highlight the potential liver-specific oncogenic role of Rictor, supported by the following evidence: First, Villanueva et al. reported chromosomal gains of RICTOR in 25% of HCC patients [23], a ratio higher than in other cancer types, such as neuroendocrine prostate cancer (~ 19%), lung cancer (~ 15%), sarcoma (~ 10%), and stomach adenocarcinoma (~ 6%) as analyzed by Kim et al. [26]. This evidence concerns the gene TP53 and lung carcinoma.